However, this is a highly non-linear process: these centers can correctly repair breaks at a certain rate, but as the break rate increases, the error rate of the repair process goes up drastically.
This seems like a surprising claim to me. I don’t see how “repair at a certain rate” would happen in the underlying biology. On the other hand, I would expect that some error are of a quality that the error detection mechanisms don’t catch them.
Our bodies are equipped with damage repair systems that are pretty darn effective at low dose rates. If this were not the case, then life would never have evolved as it has. Life started about 3 billion years ago when average background radiation was about 10 mSv/y, about 4 times the current average. Life without repair mechanisms would be impossible. But these repair mechanisms can be overwhelmed by high dose rate damage.
The repair mechanisms take a bewildering number of forms, all of which seem to have names requiring a dictionary. And the strategies are remarkably clever. At doses below 3 mSv, a damaged cell attempts no repair but triggers its premature death. However, at higher doses, it triggers the repair process.23 This scheme avoids an unnecessary and possibly erroneous repair process when cell damage rate is so low that the cell can be sacrificed. But if the damage rate is high enough that the loss of the cell would cause its own problems, then the repair process is initiated. This magic is accomplished by activating/repressing a different set of genes for high and low doses.[143][page 15] LNT denies this is possible.
Even at the cell level, the repair process is fascinating. In terms of cancer, we are most interested in how the cell repairs breaks in its DNA. Single stand breaks are astonishingly frequent, tens of thousands per cell per day. Almost all these breaks are caused by ionized oxygen molecules from metabolism within the cell. MIT researchers observed that 100 mSv/y dose rates increased this number by about 12 per day.[114] Breaks that snap only one side of the chain are repaired almost automatically by the clever chemistry of the double helix itself.
The interesting question is: what happens if both sides of the double helix are broken? Double strand breaks (DSB) also occur naturally. Endogenous, non-radiogenic causes generate a DSB about once every ten days per cell. Average natural background radiation creates a DSB about every 10,000 days per cell.[50] However the break was caused, the DNA molecule is split in two.
Clever experiments at Berkeley show that the two halves migrate to “repair centers”, areas within the cell that are specialized in putting the DNA back together.[105] Berkeley actually has pictures of this process, Figure 4.15 which is a largely complete in about 2 hours for acute doses below 100 mSv and 10 hours for doses around 1000 mSv. These experiments show that if a “repair center” is only faced with one DSB, the repair process rarely makes a mistake in reconstructing the DNA. But if there are multiple breaks per repair center, then the error rate goes up drastically. A few of these errors will survive and a few of those will result in a viable mutation that will eventually cause cancer. The key feature of this process is it is non- linear. And it is critically dose rate dependent. If the damage rate is less than the repair rate, we are in good shape. If the damage rate is greater than the repair rate, we have a problem.
The Berkeley work was part of the DOE funded Low Dose Radiation Research Program. Despite the progress at Berkeley and other labs and bipartisan congressional support, DOE shut the program down in 2015. When the DOE administrator of the program, Dr. Noelle Metting, attempted to defend her program, she was fired and denied access to her office. The program records were not properly archived as required by DOE procedures.
Footnote 23 says:
To be a bit more precise, some repairs can only take place in the G2 phase just before cell division. Radiation to the cell above 3 mSv, activates the ATM-gene, which arrests the cell in the G2 phase. This allows time for the repair process to take place.
This seems like a surprising claim to me. I don’t see how “repair at a certain rate” would happen in the underlying biology. On the other hand, I would expect that some error are of a quality that the error detection mechanisms don’t catch them.
Does anybody know more details?
So here is the relevant excerpt, section 4.7.1:
Footnote 23 says: